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M M Binns

Publications and source records attributed to M M Binns.

At least 37 records · Page 2Linked to original sources
PubMed1999

Reciprocal chromosome painting reveals detailed regions of conserved synteny between the karyotypes of the domestic dog (Canis familiaris) and human.

The domestic dog is increasingly being recognized as a useful model for human disease. The aim of this study was to conduct the first detailed whole-genome comparison of human and dog using bidirectional heterologous chromosome painting (reciprocal Zoo-FISH) analysis. We used whole-chromosome paint probes produced from degenerate oligonucleotide-primed PCR amplification of high-resolution bivariate flow-sorted human and dog chromosomes. No fewer than 68 evolutionarily conserved segments were identified between the dog and the human karyotypes. The use of elongated metaphase chromosomes for both species allowed the boundaries of each evolutionarily conserved segment to be determined to subband resolution. The distribution of conserved segments is discussed, as are the applications of these data in refining the current status of the dog genome map.

Animals↗
PubMed1999

Molecular analysis of a spontaneous dystrophin 'knockout' dog.

We have determined the molecular basis for skeletal myopathy and dilated cardiomyopathy in two male German short-haired pointer (GSHP) littermates. Analysis of skeletal muscle demonstrated a complete absence of dystrophin on Western blot analysis. PCR analysis of genomic DNA revealed a deletion encompassing the entire dystrophin gene. Molecular cytogenetic analysis of lymphocytes from the dam and both dystrophic pups confirmed a visible deletion in the p21 region of the affected canine X chromosome. Utrophin is up-regulated in the skeletal muscle, but does not appear to ameliorate the dystrophic canine phenotype. This new canine model should further our understanding of the physiological and biochemical processes in Duchenne muscular dystrophy.

Animals↗
PubMed1999

Localization and characterization of nucleotide sequences from the canine Y chromosome.

We previously reported the identification of a male-specific 658-bp DNA sequence in dogs. We used a specific primer pair designed for PCR amplification of this fragment with DNA samples from 238 dogs, 6 dingoes and 12 wolves. All 133 male samples amplified the 658-bp sequence, whereas all female samples did not. The sequence was not amplified from male DNA samples representing other wild canids (jackals, coyotes, foxes). A lambda phage was isolated from a canine male genomic library that contained an insert of approximately 15 kb of canine genomic DNA, including the male-specific 658-bp sequence. This lambda phage was used in fluorescence in-situ hybridization experiments. It hybridized to the canine Y chromosome together with a lambda clone containing a segment of the SRY gene and a cosmid clone containing a portion of the pseudoautosomal region. The male-specific 658-bp sequence was located at the end opposite to the pseudoautosomal region while the SRY gene sequence hybridized near the centromere. Additionally, two (CA)-repeat sequences were identified in the lambda clone that contained the 658-bp sequence. Specific primer pairs were designed to amplify each of the repeats. Primer pair MS34 amplified three different alleles from 13 unrelated canine male DNA samples with a PIC value of 0.40. Primer pair MS41 amplified five alleles with a PIC value of 0.71. These microsatellites are the first reported polymorphic sequences in the dog located in the non-recombining portion of the Y chromosome.

Animals↗
PubMed1999

Seven new linkage groups assigned to the DogMap reference families.

Twenty microsatellite markers have been typed on to the DogMap reference families, of which 18 were found to be polymorphic. One marker has been assigned to an existing linkage group and nine others have formed seven new linkage groups with previously typed markers. Only one of the new groups could be ordered.

Animals↗
PubMed1999

Report of the International Equine Gene Mapping Workshop: male linkage map.

The goal of the First International Equine Gene Mapping Workshop, held in 1995, was the construction of a low density, male linkage map for the horse. For this purpose, the International Horse Reference Family Panel (IHRFP) was established, consisting of 12 paternal half-sib families with 448 half-sib offspring provided by 10 laboratories. Blood samples were collected and DNA extracted in each laboratory and sent to the Lexington laboratory (KY, USA) for dispatch in aliquots to 14 typing laboratories. In total, 161 markers (144 microsatellites, seven blood groups and 10 proteins) were tested for all families for which the sire was heterozygous. Genealogies and typing data were sent for analysis to the INRA laboratory (Jouy-en-Josas, France) according to a specific format and entered into a database with input verification and output processes. Linkage analysis was performed with the CRIMAP program. Significant linkage was detected for 124 loci, of which 95 were unambiguously ordered using a multipoint analysis with an average spacing of 14.2 CM. These loci were distributed among 29 linkage groups. A more comprehensive analysis including synteny group data and FISH data suggested that 26 autosomes out of 31 are covered. The complete map spans 936 CM.

Animals↗
PubMed1999

Genetic mapping of the copper toxicosis locus in Bedlington terriers to dog chromosome 10, in a region syntenic to human chromosome region 2p13-p16.

Abnormal hepatic copper accumulation is recognized as an inherited disorder in man, mouse, rat and dog. The major cause of hepatic copper accumulation in man is a dysfunctional ATP7B gene, causing Wilson disease (WD). Mutations in the ATP7B genes have also been demonstrated in mouse and rat. The ATP7B gene has been excluded in the much rarer human copper overload disease non-Indian childhood cirrhosis, indicating genetic heterogeneity. By investigating the common autosomal recessive copper toxicosis (CT) in Bedlington terriers, we have identified a new locus involved in progressive liver disease. We examined whether the WD gene ATP7B was also causative for CT by investigating the chromosomal co-localization of ATP7B and C04107, using fluorescence in situ hybridization (FISH). C04107 is an anonymous microsatellite marker closely linked to CT. However, BAC clones containing ATP7B and C04107 mapped to the canine chromosome regions CFA22q11 and CFA10q26, respectively, demonstrating that WD cannot be homologous to CT. The copper transport genes CTR1 and CTR2 were also excluded as candidate genes for CT since they both mapped to canine chromosome region CFA11q22. 2-22.5. A transcribed sequence identified from the C04107-containing BAC was found to be homologous to a gene expressed from human chromosome 2p13-p16, a region devoid of any positional candidate genes.

Adenosine Triphosphatases↗
PubMed1999

Zoo-FISH analysis of dog chromosome 5: identification of conserved synteny with human and cat chromosomes.

Conserved segments of synteny between the human genome and chromosome 5 (CFA 5) of the domestic dog (Canis familiaris) have been identified by reciprocal chromosome painting analysis. A CFA 5 paint probe was applied to human metaphase spreads, revealing distinct hybridisation sites on human (HSA) chromosomes 1, 11, 16, and 17. Paint probes for these human chromosomes were then hybridised to dog metaphase spreads, identifying the regions of CFA 5 with which homology is shared with the corresponding human chromosome. Application of the CFA 5 paint probe to metaphase spreads of the domestic cat (Felis catus, FCA) demonstrated hybridisation to cat chromosomes C1, D1, E1, and E2. Dog PCR primers for type 1 markers known to lie in the corresponding regions of HSA 11, 16, and 17 were used to isolate dog BAC clones representing four genes. Fluorescence in situ hybridisation analysis confirmed their localisation to CFA 5 and suggested that two of the conserved segments lie in opposing orientations on CFA 5, compared to the human chromosome concerned. A third segment appears to lie in the same orientation on both human and dog chromosomes. No suitable gene markers were available for analysis of the fourth segment. The significance of these findings is discussed with reference to current and future dog genome mapping efforts.

Animals↗
PubMed1998

DNA marker C04107 for copper toxicosis in a population of Bedlington terriers in the United Kingdom.

The DNA microsatellite marker C04107, linked to the Bedlington terrier copper toxicosis locus, is used diagnostically in the USA to detect the disease allele. This marker has been typed in Bedlington terriers of known disease status in the United Kingdom, and it is concluded that it should be useful in eradicating the disease from the breed in the UK. The marker also identified a dog which had been diagnosed on the basis of a liver biopsy as having the disease, as being unaffected; a second liver biopsy confirmed that the dog did not have copper toxicosis.

Animals↗
PubMed1998

A comparative genetic analysis of the Irish greyhound population using multilocus DNA fingerprinting, canine single locus minisatellites and canine microsatellites.

Pairwise analysis of HinfI/33.6 DNA fingerprints from a total of one hundred and fifty-three Irish greyhounds of known pedigree were used to determine band-share estimates of unrelated, first-degree and second-degree relationships. Forty-eight unrelated Irish greyhounds were used to determine allele frequencies for three single-locus minisatellites, and following a preliminary screen, eight of the most polymorphic tetra-nucleotide microsatellites from a panel of 15. The results indicated that both band-share estimates by DNA fingerprinting and microsatellite allele frequencies are highly effective in resolving parentage in this greyhound population, while single-locus minisatellites showed limited polymorphism and could not be used alone for routine parentage testing in this breed. The present study also demonstrated that, to obtain optimal resolution of parentage, sample sets of known pedigree status are required to determine the band-share distribution and/or microsatellite allele frequencies.

Animals↗
PubMed1997

Genetical and physical assignments of equine microsatellites--first integration of anchored markers in horse genome mapping.

Twenty equine microsatellites were isolated from a genomic phage library, and their genetical and physical localization was sought by linkage mapping and fluorescent in situ hybridization (FISH). Nineteen of the markers were found to be polymorphic with, in most cases, heterozygosities exceeding 50%. The markers were mapped in a Swedish reference family for gene mapping, comprising eight half-sib families from Standardbred and Icelandic horse sires. Segregation was analyzed against a set of 35 other markers typed in the pedigree. Thirteen of the microsatellites showed linkage to at least one other marker, with a total of 21 markers being involved in these linkages. In parallel, 18 of the microsatellites could be assigned to their chromosomal region by FISH. These assignments involved eight equine autosomes: ECA1, 2, 4, 6, 9, 10, 15, and 16. The genetical and physical mappings revealed by this study represent a significant extension of the current knowledge of the equine genome map.

Alleles↗
PubMed1997

A survey for antibodies to equine arteritis virus in donkeys, mules and zebra using virus neutralisation (VN) and enzyme linked immunosorbent assay (ELISA).

A seroepidemiological survey of donkeys in South Africa (n = 4300) indicated a wide distribution and increasing prevalence of antibodies to equine arteritis virus (EAV). Donkey sera inhibited equine arteritis virus infection in virus neutralisation (VN) tests and in ELISA specifically bound to a recombinant antigen derived from the Bucyrus isolate of EAV. These results suggest that donkeys have been exposed to the same serotype of this virus as circulates among horses. A good correlation existed between EAV neutralising antibody titres and ELISA absorbance values (0.8631); the ELISA was sensitive and specific (99.2% and 80.3% respectively) for donkey sera when compared to the VN test and the recombinant ELISA antigen did not cross-react with sera positive for common African equine pathogens. VN+ ELISA+ donkeys were also found in Morocco and Zimbabwe and seropositive mules in both South Africa and Morocco. No seropositive zebra (n = 266) were detected from game reserves or zoos in 9 countries. The results confirm that in addition to horses and donkeys, mules are naturally infected with EAV.

Animals↗